Pulmonary emphysema is a devastating disease causing progressive destruction of lung tissue, resulting in respiratory failure. The primary target of tissue injury appears to be elastic fibers. These fibers are degraded by elastases that accumulate in the lung as a result of chronic inflammation brought on by cigarette smoking, air pollutants, infections, and other factors. Since emphysema is related to elastic fiber damage, measurement of the rate of breakdown of these fibers may be useful in assessing the progression of the disease. To date, attempts to measure elastic fiber breakdown products have involved sampling of blood, urine, tracheal aspirates, and bronchoalveolar lavage fluid. The use of blood or urine is complicated by the fact that both fluids contain elastic fiber breakdown products from tissues other than the lung, including elastic fiber-rich tissues such as blood vessels and cartilage. Consequently, diseases such as arteriosclerosis or osteoarthritis may obscure the component of elastic fiber injury due to pulmonary emphysema. The use of tracheal aspirates and bronchoalveolar lavage removes this complication, but the procedure entails a significant degree of patient discomfort and is therefore unsuitable for repeated measurements.
The only source of elastic fiber breakdown products that is readily accessible and specific for lung injury is sputum. The presence of elastic fibers in the sputum of patients with necrotizing pneumonia is well-documented (1–3). However, the quantitative measurement of elastic fiber breakdown products in sputum has not been previously attempted, nor has there been any correlation between the levels of these breakdown products in sputum and degree of lung injury.